Talk:Imprinted brain hypothesis

why is the Crespi paper not good enough?
I would keep the information but reframe it as a summary of Crespi's findings. Jonathan Tweet (talk) 23:06, 18 January 2019 (UTC)

pseudoscience?
A recent rewriting of this page claims the theory is pseudoscience, and attempts to debunk crespi & badcock's claims. Most of what was written is either misrepresentation of their claims, or has weak or unsupporting citations

This page incorrectly portrays the imprinted brain theory as being autism vs schizophrenia, completely neglecting the autistic and psychotic spectrums which it really proposes are diametrical, these spectrums whose existence is supported in modern psychiatry, such as with The Hierarchical Taxonomy of Psychopathology, a new diagnostic model towards psychotic-affective spectrum disorders closely resembling the spectrum proposed by crespi & badcock. The claim it "lacks scientific backing" is cited with a thesis (Suzanna Russell-Smith, 2012) which tests a few hypotheses of the imprinted brain theory. The results of these tests are all in support, except for one which found a significant correlation between the O-LIFE and autism quotient, which are self report measures for schizotypal and autistic traits, which does not disprove the theory or provide quality counter evidence as psychotic social and cognitive deficits may superficially resemble each other. Crespi & Badcock (2008) did not claim that schizotypal personality disorder leads to enhanced theory of mind, rather the claim was that "healthy schizotypy" (the concept proposed by Gordon Claridge, where moderate positive schizotypy in the absence of disorganized and negative schizotypy, in the absence of a mental disorder may lead to positive outcomes. The citation that claimed to refute this only found negative schizotypy is associated with decreased theory of mind ability, but positive schizotypy was not. Comorbidity does not reflect shared etiologies, and diagnosis is based on description of phenotypes rather than objective etiologies. Childhood autism which leads to psychosis is most likely a misdiagnosis, as childhood schizotypal disorder is a neglected diagnosis (Tonge et al. 2020). Crespi & Badcock do not claim schizophrenia spectrum disorders have "intensified empathy and strong theory of mind", rather they claim that cognitive empathy is "over-developed" and as such inaccurate. Intact affective empathy in autism & schizophrenia is essentially unrelated to what crespi & badcock claim, as their focus is on under-developed vs over-developed cognitive empathy, not emotional response. Superficial overlap of symptoms does not mean shared etiology. For example, increased dopamine and decreased dopamine can both lead to increased social anxiety. The common cold and polio if treated this way would be said to be very similar conditions due to similar symptom profile, however if using crespi & badcock's method of looking at the underlying causes behind the dysfunction, you would find that polio and the common cold are completely different infections. Studies on symptom overlap in schizophrenia and autism have found, as predicted by the diametrical model, that symptoms such as paranoia present differently in autism than they do in schizophrenia (Pinkham et al. 2012) Cognitive problems are found in both autism and schizophrenia, but these oppose each other, and this has been found for a wide range of functions, such as local-global processing, circumspect vs jumping to conclusions reasoning bias, rigid semantic networks vs chaotic semantic networks, lower susceptibility to rubber hand illusion vs higher, enhanced stroop task performance vs reduced, over-selective attention vs over-inclusive attention, decreased inattentional blindness vs increased, rotational > verbal skills vs verbal > rotational skills. All of these findings and more can be found in papers independently from the ones by Badcock & Crespi. — Preceding unsigned comment added by Cloudpostings (talk • contribs) 03:53, 28 January 2021 (UTC) — Cloudpostings (talk&#32;• contribs) has made few or no other edits outside this topic.

Healthy schizotypy is positive schizotypy in the absence of other schizotypy dimensions, and with intact mental health. Studies measuring healthy schizotypy must control for these variables or they are not measuring healthy schizotypy. The citation provided did not control for these variables. Again, they never claimed schizotypal personality disorder improved empathetic or theory of mind accuracy. Emotion recognition is also impaired (however its found high schizotypes actually over exaggerate others facial expressions, supporting hyper-mentalism) Crespi & Badcock do not claim schizotypes are better at empathy. Even so, its a very minor line of evidence for the theory Cloudpostings (talk 21:23, 27 January 2021 (UTC) — Cloudpostings (talk&#32;• contribs) has made few or no other edits outside this topic.


 * Thanks for raising your concerns. For what it's worth, you've formatted this objection wrong, so it's a nearly unreadable wall of text. Use double spacing, not single spacing, to make new lines.
 * Past that, the objections you raise are for the most part irrelevant; the ones that are relevant have since been addressed or are being addressed. For instance, your claim that schizophrenic children and adults with ASDs do not have ASDs is original research, which is not allowed on Wikipedia. Tonge et al. does not make the claim you used it to support here, in that while it proposes that schizotypal disorder in childhood is a distinguishable disorder from ASD, it doesn't claim that 'schizo-autism' is in fact an entirely schizophrenia-spectrum diagnosis. (It also, to my eye, conflates MDI and MCDD quite a bit when they have significantly different profiles, but that's another topic.) Additionally, your claim regarding the irrelevance of affective empathy is in turn irrelevant to anything in the article; the section in question is noting that both conditions cause decreased cognitive empathy, and in particular that the deficit is specific as to cognitive empathy rather than a global deficit, quite the opposite of an opposing issue. Similarly, your notes about positive schizotypy and emotional recognition are irrelevant to the current state of the article, which explicitly cites that people with high positive 'healthy' schizotypy have impaired emotional recognition from faces. (The 'intensified empathy' wording you object to is from the original version of the article, so I can't answer to it; I'm not entirely happy with that wording, but can't find a smooth replacement that explains the claim to a general/non-medical audience.)
 * The degree to which cognitive problems in autism and schizophrenia 'oppose each other' is hotly debated, and something where putting the entire body of literature into this article would result in an overlong and bloated mess. Suffice to say, the simple claim you've made here is not backed up by the modern state of research. (I'm currently brainstorming an 'Autism and schizophrenia' article to address content that's currently split between maybe five or six different articles, which will be the correct place to go in-depth on where and how the cognitive profiles of autism and schizophrenia are in and out of sync.) In particular, your claim regarding VIQ>PIQ and PIQ>VIQ profiles is completely bunk in recent research, in which not only is the traditional autistic PIQ>VIQ profile only the case in one subset of the autistic population, but it also occurs in a subset of the schizophrenic population. (The former is at this point very well-known, but the latter may be unfamiliar to you -- see here if you're doubting me.)
 * I note you've avoided the parts of the article that discuss etiological refutation of the hypothesis, such as the problems posed by imprinting disorder phenotypes. My experience with the imprinted brain hypothesis on this note is consistently to either entirely ignore the issue or to make completely false claims about the phenotypes of these disorders (as Crespi indeed does). I can't seriously consider an objection based around "the phenotypic similarities don't mean the etiologies are in question" that avoids the matter of the etiologies actually being in question. Simultaneously, the claim that the imprinted brain hypothesis is about conditions other than ASDs and SSDs is contingent on those predictions being correct; when they've been falsified, the claim falls apart.
 * I also note that your only edits to Wikipedia appear to be on this article. I recommend you read the project page Single-purpose account to familiarize yourself with how this is perceived on Wikipedia, as well as WP:NOTHERE for further discussion of why SPAs (as they're called for short) are considered such an issue.
 * Thanks for coming here to raise your concerns rather than attempting to edit-war the article. I hope you have a good day. Also, for future reference, new talk page sections should be added at the end rather than the beginning. I've fixed that for you here. Vaticidalprophet (talk) 04:32, 28 January 2021 (UTC)


 * Angkustsiri et al. (2014) review evidence that ASD diagnoses in 22q11.2 deletion syndrome are likely false positives, and the social impairments are different from idiopathic ASD. Schizophrenia in turner syndrome patients almost exclusively occurs in turner patients with a mosaic karyotype (Jung et al. 2014), and autism occurs mostly in turner patients who inherited the maternal x chromosome (Skuse et al. 2008), which is compatible with the imprinted brain theory as males inherit the x chromosome from their mother (Crespi, 2008). Autism in klinefelter syndrome seems to be characterized by speech delay and introversion without repetitive behavior or intense interests (Crespi, Summers, Dorus, 2009). Trisomy x doesn't seem to have an elevated prevalence of autism (Bishop et al. 2011), the source provided on the wiki page for trisomy x doesn't report on the prevalence of autism in trisomy x.
 * Studies cited to claim theory of mind, or more accurately mentalizing is reduced in schizophrenia don't support the claim, they support that ToM and mentalizing are impaired, but none study whether schizophrenics hyper-mentalize as the diametric model predicts, however ones that do study Badcock & Crespi's actual implications have found the predicted results of the diametric model (Bara et al. 2011)(Clemmensen et al. 2014)(Ciaramidaro et al. 2015)(Stanfield et al. 2017)(Abu-Akel, Bailey, 2000)
 * Its claimed that "biological opposition of schizophrenia and autism is not supported by research" but the citations for this are studies in which the behavioral phenotypes of autism and schizophrenia co-occur, which doesn't address biologial cause, and in the imprinted brain theory model the authors repeatedly address that apparent co-morbidity may really be false positives, which phenotypic co occurence of behaviors does not address.
 * The dismissal of this theory as being pseudoscience based on 1) apparent comorbidity which the authors have acknowledged from the beginning 2) misrepresentation of how Crespi & Badcock conceptualize these disorders. The claim this theory is "not backed by science" is erroneous, not only is there no citations of any studies refuting aspects about the imprinted brain theory, there is a massive amount of evidence (much of which is more recent) confirming predictions of this model (more examples; Robbins & Jack (2006)Lopez-Tobon et al. (2020)Warrier et al. (2018)Crespi et al. (2018)Hypo-mechanismLindeman & Lipsanen (2016)Faust & Kenett (2014)). — Preceding unsigned comment added by Cloudpostings (talk • contribs) 08:59, 28 January 2021 (UTC)  — Cloudpostings (talk&#32;• contribs) has made few or no other edits outside this topic.


 * Working through this as I go:
 * Angkustsiri et al (2014) strikes me as frankly a singularly unconvincing study, which is unfortunate, because I was hoping I could use it here as an example of people disputing the VCFS autism effect. It continues to find a far above average rate of autism symptomatology, and the decision to paint this as "no autism increase" seems linked to narrow and outdated views of ASDs, such as the aforementioned PIQ>VIQ myth.
 * The point you keep reiterating about false positives is an example of the unfalsification criticism. Crespi and Badcock not only evade the matter of what clinical presentations provide evidence against their hypothesis, they lean further into claims such as "this is a spurious diagnosis" as examples pop up. Similarly, the majority of the 'recent evidence' you give provides nohing not contradicted anywhere, with the only study of genuine interest being Warrier et al -- and even then the findings give me pause, considering that anorexia nervosa (which is strongly associated with autism and autistic symptomatology) also turns out on the 'anticorrelated' end. Considering the relative sex ratios of ASD and AN, and that the most sex-equal SZ has the weakest correlation (and it's honestly pretty weak), I would wonder to what degree the results are corrupted by EQ's sexual dimorphism.
 * "Not supported by research" is the beginning of an entire section which goes into many issues, including ones that I've noted you're conspicuously ignoring. It is also not the same thing as "disproven by research". For the most part, the imprinted brain hypothesis is unsupported, and most of the findings in its favour even in this relatively narrow selection you give are related to or presented by Crespi and Badcock. Many of the claims for its support -- like the ones you make yourself -- are goalpost-shifting, claiming poor diagnosis and otherwise erasing the possibility of genuine confluence. A lot of the evidence you (and C&B) give in your favour (and which is given in favour of the hypothesis more generally) is also from fMRI studies, which are singularly difficult to draw conclusions about; brain structure studies tend to come up very differently.
 * Sex chromosome trisomy (not technically an accurate term for XYY and XXY, but you know what I mean) is associated with autism in all cases, which is touched on by the review and mentioned more in-depth in a new cite. "Autism in 45,X is overwhelmingly associated with maternal inheritance" is unconvincing on the note that 45,X is overwhelmingly associated with maternal inheritance, and current data does not support that autistic women have a far higher prevalence of it. The mosaicism/SZ association is interesting and something I've considered myself, but I don't believe it lends support to specifically this hypothesis rather than general effects of the X chromosome in schizophrenia.
 * Overall, what you present simply does not lend credence to the suggestion here in the context of the overall body of research; it's lower-quality, question-begging, and notably evading important issues like "why do higher-quality forms of neuropsychiatry find the opposite?" or "why do imprinting disorders completely violate the predictions made here?". I can recognize the position that the article is currently too biased against the hypothesis -- but see WP:FRINGE and WP:UNDUE -- and am working to soften some wording. But, overall, what you propose here just isn't relevant to the page.
 * Also, I notice you've been tagging many major content-changing edits, including the comment I'm replying to, as 'minor edits'. Have you read WP:MINOR? Vaticidalprophet (talk) 09:51, 28 January 2021 (UTC)


 * The mentioning of false positives is not erasing possibilties of genuine confluence, however they cannot be taken as proof that the theory is wrong until the presentation of these diagnoses in these conditions is examined critically, to claim these cases are definitely false positives or definitely not false positives is baseless. The theory is definitely by no means "proven" but there is no justification for dismissing it completely as pseudoscience because of that. The theory should be presented as it is, with accurate portrayal of the authors claims as well as criticisms, rather than presenting only criticisms and only presenting few examples of supporting evidence worded in such a way that its implied to be wrong, and overall misrepresenting many aspects about the theory. Opposites in the correlated phenotypes of ASD and PSD are completely neglected despite them being a large part of the evidence for the diametrical ASD-PSD model, as well as considerations for biological etiologies (such as oxytocin & testosterone), and pharmacological aspects of the model (such as diametrical treatment with mGlur5 antagonists vs agonists for ASD and PSD respectively). Cloudpostings (talk) 10:55, 28 January 2021 (UTC) — Cloudpostings (talk&#32;• contribs) has made few or no other edits outside this topic.

(For the record, "the theory is by no means proven" means it isn't a theory in the scientific sense...)

The article gives accurate portrayals of the authors' claims. It also describes -- as I have repeatedly mentioned -- the biological claims and the way the evidence falls for the biological claims. Perhaps it should discuss hormonal matters more, yes; the article is not in fact finished and I'm continuing to collate information. Ultimately, you seem to just be going in circles and trying to backfill evidence for yourself. Most of what you've either added or proposed has been some combination of "low-quality evidence", "misinterpreted", and "NPOV violation" -- which is exactly what state the page was previously in. I've worked to improve the wording of supporting evidence that you seem to interpret as "claiming it's doing something wrong", though I'm unconvinced you're making this claim in good faith. I'm also concerned about the possibility you have a conflict of interest regarding this article, especially considering you made an account solely to participate in this issue. Vaticidalprophet (talk) 11:08, 28 January 2021 (UTC)

Also, I'm guessing one of your primary issues with the article is the infobox? The problem is that Template:Infobox pseudoscience is the only infobox relating to scientific hypotheses (check the recent edit history of me reverting myself trying to fix it...). I don't quite like having the caption there, because as you point out, whether the hypothesis is pseudoscience or not is something reasonable people can disagree on. However, I can't actually remove it at this time, because the template to do so does not exist. Vaticidalprophet (talk) 11:12, 28 January 2021 (UTC)


 * The idea that schizophrenia is characterized by simple "deficits" in empathy is incredibly reductionist, and is treated similar to how autism is (eg, "autistic people don't have emotions" based on subjective judgement of someone without the condition, instead of listening to autistic people who describe having strong emotions but being unable to express their emotion in the same way as neurotypicals). Furthermore, claims of schizophrenics simply having simple reduced theory of mind is based on their performance on less than objective tests which rely on common sense ideas of what an action means, without considering how they actually think about others minds and intentions, and therefore cannot be taken alone as proof that they have simply "reduced" theory of mind.
 * As Crespi has mentioned in his papers, the interpretation of psychiatric symptoms currently is subjective and deviations from the norm are labeled "deficits" or purely pathological symptoms. Phenomenological studies on schizophrenia are lacking, so currently there are few studies which touch on the phenomenology of empathy in schizophrenia (that support "hyper-mentalzing"), but shuts down the voices of actual schizophrenics who describe themselves as "thinking too much about what caused a person to do something" being "being better at understanding others viewpoints even when disagreeing with them", tolerating abuse against them because "its not inherently their fault because I can understand what caused them to do it". Obviously without a controlled study (which I will link to several of) this can't be considered the experience of every schizophrenic, but makes the claims of reduced empathy necessary to be re evaluated.
 * Phenological studies do not support reduced theory of mind as being a feature of schizophrenia. Schizophrenics think too much about others minds and their own minds, to the point where they are intensively aware of how others perceptions and the perceptions of ones self are subjective and based on internal psychological factors, and as a result reject folk ideas of morality, common sense, etc because they are overly aware of how a "good" or "bad" person is based on subjective ideas of good or bad, and actions of others are not based on inherent "essence" of people but their feelings, thoughts, and experiences, which makes anything inherently uncontrollable (Stanghellini & Ballernini 2007). Mentalizing is described as "understanding misunderstanding", and too much mentalizing can explain most aspects of the schizophrenic experience. Its important to not think of mental processes as exerting effects short term, but they are the basis for learning and mental development, so the assumption that atypical interpretation of others behavior is not a result of a different state (or even necessarily wrong), but has a basis in ones entire lifetime of learning and thinking. Being able to relate to others is not simply an inability to percieve other peoples mental states, but rather it could indicate that the way you experience life is radically different from others. People with schizophrenia do not have "common sense", that is the unquestioned, automatic comprehension of things and considering them to be self evident, meaning people with schizophrenia are focused on knowing what's "behind the curtains", especially in regards to other peoples behavior and thinking, and also question why other people believe in social constructs that aren't real and act on these social constructs (Stanghellini & Ballernini 2007).
 * Its an obvious consequence that over-mentalizing, that is understanding misunderstanding and knowing what's "behind the curtains" in other's minds would go to the extent where one realizes that emotions and beliefs are nothing more than socially imposed ideas and evolutionary adaptations selected to guide human behavior for the purpose of reproduction and survival. To mentalize is to find the cause of a behavior, and going far enough the eventual conclusion is determinism. Not many studies have tested the relationship between empathy and belief determinism, but one study says they are connected.. Looking at moral beliefs in autism, the reverse pattern is seen from schizophrenia: autistic individuals tend to judge something as moral based on whether the action violates a moral code, rather than the psychological factors that caused the action, and people who had perspective taking intact did so based on evaluating the cause of a person's action (Fadda et al. 2016). Furthermore, the study indicates that moral judgement in autism is based on common sense ideas of morality, which is opposite to the rejection of common sense in schizophrenia. In an test of perspective taking which was made to be more objective than the ones cited to claim schizophrenics lack theory of mind, schizophrenics are better on seeing other person's perspectives (Abu-Akel et al. 2015). Schizophrenics are also hyper-reflective and think too much about their own minds as well, which is a fundamental process involved in mentalizing, as the awareness of your own minds ability to misunderstand means you are aware that others minds are also fallible to misunderstanding.
 * Before this is dismissed as being original research, I'm not making synthesis to claim that schizophrenics are hypermentalizers. Rather it is against your claim that because schizophrenics do poorly on non-objective measures of mentalizing (which are based on an older, non objective understanding of what mentalizing objectively is), all the lived experience, phenomological, genomic, neurological, and objective evidence, can be discarded, and new theories are wrong because tests of a completely different concept of "mentalizing" don't support the theory. Crespi & Badcock never claimed schizophrenia is caused by higher accuracy at judging emotional states, higher accuracy at accurately perceiving facial expressions, higher accuracy at theory of mind tasks, etc, which they explicitly claimed would be impaired by hyper-mentalizing, not enhanced. Goal post shifting is not the same as acknowledging the semantic origins of a claim. There is far from any sort of "settled science" in psychiatry, and new ideas which question the basic assumptions that are held in current psychiatry are necessary for scientific progress, and appeals to authority "higher quality forms of neuropsychiatry find the opposite" are exactly what prevents scientific progress. This article reports exclusively from older and traditional views of psychiatry without acknowledging the assumptions and semantics being challenged by the imprinted brain theory, in such that claims said as "not supported" with not acknowledging what the claim means (eg, that autism and schizophrenia are opposites are talking about these disorders as their subjective broad symptoms which are used for diagnosis, instead of their actual claim being that the phenotypes of most people diagnosed with autism or schizophrenia are caused by opposite patterns of maladaptation).
 * The etiological refutations, as I've said before aren't objective and are based on the diagnosis of social deficits as autism, and the assumption that these diagnoses are objectively real, which is by no means an invalid criticism or deflecting of refutation, rather its rational skepticism towards the unquestioned assumption that they are objectively real (and they're not, if they were etiologically defined diseases there would be no need to debate about their causes anymore). Mentalizing is in fact, impaired in radically different ways, if looking not just at performance on basic tasks, but the consequences of hypo vs hyper mentalizing (such as attitudes towards morality). The claim that schizophrenics have reduced oxytocin levels means that elevated oxytocin can't be involved in the development of schizophrenia is not logically sound, as social isolation is known to cause reduced oxytocin, and it is about elevated levels or reactivity in development of schizophrenia, not a continuous state of high oxytocin. Cloudpostings (talk) 02:57, 25 February 2021 (UTC)


 * I'm wildly amused by the implications I align with traditional psychiatry or with the idea autistic people don't have emotions, but that's neither here nor there. Let's cut to the chase: the fact you didn't get the reaction you wanted on /r/evolutionarypsychology is no reason to think you're going to find it on Wikipedia. You are running yourself in circles to justify the hypothesis and in the process alluding to things that actively make them less likely to appear in Wikipedia articles, not more -- the process of Wikipedia is extremely, and by design, biased towards settled science and against new theories. (This is actually something I have my own problems with, but such is such.) I'm also not the world's biggest fan of the apparent impression running through your posts that this is the cutting-edge lived-experience-respecting position, because the single biggest problem with the imprinted brain hypothesis -- far more than anything this article can discuss -- is that it so wildly contradicts people's lived experience. But that is again neither here nor there, and just as far outside Wikipedia's scope as "we need to challenge traditional psychiatry's assumptions!" is.
 * You are not addressing the things I've asked you to address (why do people with Prader-Willi syndrome have obviously autistic phenotypes and not schizophrenia phenotypes; why do the maternally overimprinted ones have those even moreso?), and you have not provided anything at all within Wikipedia's scope. You are here to push a point of view that got laughed out of an evopsych subreddit. Let me be clear: I have been unusually polite and responsive to you, compared to what 99% of Wikipedia editors would do in this situation. Your behaviour is formally considered grounds for being blocked from editing. I have not pursued that block for your benefit.
 * You have a serious misapprehension of what the scope of Wikipedia is and of the relevance of anything you have said to it. I'm even sympathetic to aspects of that, because I too think there are places where that scope works against the pursuit of knowledge, but this is not one of them, and repeated tendentious arguing on the talk page can only backfire. I am making this extremely clear for your own benefit. If you had stumbled upon someone less patient, you would not be able to have this conversation. Vaticidalprophet (talk) 09:01, 25 February 2021 (UTC)